title: Suppression of cellular immunity in obstructive jaundice is caused by endotoxins: a study with germ-free rats.
abstract: The increased susceptibility to infections after surgery in jaundiced patients is considered to be caused by an impairment of cellular immunity and/or nutritional status. Endotoxins are suggested to play a role in the pathogenesis. However, the mechanism of action is unknown. Germ-free rats were used to study the effect of biliary obstruction in a model with negligible amounts of endotoxin. Cellular immunity, production of tumor necrosis factor (as a mediator of endotoxin toxicity) by peritoneal macrophages, and the nutritional status were assessed. Significant suppression of cellular immunity was found in conventional rats with obstructive jaundice. In contrast, cellular immunity was not suppressed in jaundiced germ-free rats. Large amounts of tumor necrosis factor were spontaneously secreted by peritoneal macrophages of jaundiced conventional rats, whereas macrophages from jaundiced germ-free rats did not. Moreover macrophage activation (expressed in tumor necrosis factor production) was significantly related to suppression of cellular immunity. Weight changes and depression of albumin levels were not different in germ-free and conventional rats after bile duct ligation. The data presented indicate that suppression of cellular immunity in obstructive jaundice is caused by endotoxins, whereas the impaired nutritional status seems to not be affected by the presence of endotoxins.
authors.affiliation: Department of Surgery, University of Limburg, Maastricht, The Netherlands.
authors.forename: J W
authors.initials: JW
authors.lastname: Greve
authors.forename: D J
authors.initials: DJ
authors.lastname: Gouma
authors.forename: P B
authors.initials: PB
authors.lastname: Soeters
authors.forename: W A
authors.initials: WA
authors.lastname: Buurman
mesh_terms: D000818:Animals; D002779:Cholestasis / Q000276:immunology*; D004731:Endotoxins / Q000633:toxicity*; D005856:Germ-Free Life / Q000276:immunology*; D007111:Immunity, Cellular; D008262:Macrophage Activation / Q000276:immunology; D008264:Macrophages / Q000276:immunology*; D008297:Male; D009752:Nutritional Status; D051381:Rats; D011919:Rats, Inbred Strains; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D004731:Endotoxins; D014409:Tumor Necrosis Factor-alpha